Lecture 14 - Nervous tissue and the neuromuscular junctions Flashcards
Neurons have the same basic structure
Dendrites Cell body Axon Axon hillock Axon terminals
CNS
brain and spinal cord
PNS
peripehral nerves
PNS divisions
Afferent division and efferent division
Afferent division of PNS
Sensory stimuli - receptors in the skin for example which convey information back to the nervous system
visceral stimuli - internal organs changes and this information gets sent back to the nervous system
Efferent division of PNS
Somatic nervous system (voluntary)
- motor neurons that innervate skeletal muscle
Autonomic nervous system (involuntary)
- sympathetic = fight or flight
- parasympathetic = rest and digest
Multipolar neurons
Multiple dendrites project from cell body (one axon)
Bipolar neurons
Single dendrite opposite from axon
Pseudo-unipolar neurons
Axon and dendrite rise from a common stem of the cell body
Cellular structure of a neuron
Large nucleus –often large, reflecting metabolic demand
Many mitochondria
Lots of ER, particularly in large neurons. Can be found in dendrites but not axons (protein synthesis in dendrites but not in the axons)
Numerous neurofilaments. Together with microtubules make up the cytoskeleton
Synapses are found at dendrites and also cell body
Central nervous system
CNS is macroscopically divided into grey matter (neuron cell bodies, dendrites and axons) and white matter (axons; many myelinated)
Effectively made of myelination that surrounds the axons
The white matter (W) in the cerebrum can be delineated with a dye with an affinity for myelin. The outer cortex (C - gray matter) is composed of nerve cells and does not contain myelin
White matter in the cerebellum is located centrally. Neuron cell bodies are located in the complex folds (folia) and stained purple in this section. (Folding optimises space in this area of the brain)
CNS white matter
white matter (axons; many myelinated)
CNS grey matter
grey matter (neuron cell bodies, dendrites and axons)
White matter in cerebrum
The white matter (W) in the cerebrum can be delineated with a dye with an affinity for myelin. The outer cortex (C - gray matter) is composed of nerve cells and does not contain myelin
White matter in the cerebellum
White matter in the cerebellum is located centrally. Neuron cell bodies are located in the complex folds (folia) and stained purple in this section. (Folding optimises space in this area of the brain)
Oligodendrocytes
CNS equivalent of a Schwann cell
Myelinate axons
Each oligodendrocyte can myelinated many different axons and therefore each axon will be myelinated by many different oligodendrocytes
Astrocytes
Provide mechanical support (also form part of the blood brain barrier)
Maintain microenvironment
Microglia
Specialised immunological cells of the CNS
Fight infections in the brain
Ependymal cells
Ciliated cuboidal epithelial cells which line the cavities of the brain and spinal cord
Peripheral nerves
A nerve consists of one or more bundles of nerve fibres called fascicles
Axons inside the fascicles are surrounded by collagenous support tissue called endoneurium
The fascicles are enclosed in dense collagenous tissue called perineurium
The fascicles are bound together by loose collagenous tissue called epineurium
Note = Schwann cells are the main support cells of the PNS
Fascicles
A nerve consists of one or more bundles of nerve fibres called fascicles
Endoneurium
Axons inside the fascicles are surrounded by collagenous support tissue called endoneurium
PErineurium
The fascicles are enclosed in dense collagenous tissue called perineurium
Epineurium
The fascicles are bound together by loose collagenous tissue called epineurium
Main support cell of the PNS
schwann cell
Myelinated and non-myelinated fibres
Peripheral nervous system axons are enveloped by Schwann cells, providing structural and metabolic support.
Large and small diameter fibres differ in the degree to which they are enveloped:
Small – non-myelinated
Large – myelinated
Non-myelinated nerves
Small diameter axons of the autonomic system and small pain fibres are simply enveloped by the cytoplasm of Schwann cells.
Enveloped by the cytoplasm that effectively closes back over and almost connects back with itself in something known as the mesaxon
Myelinated nerves
The axon is invaginated into the Schwann cell cytoplasm
The outer membrane of the Schwann cell fuses to form a mesaxon
The mesaxon rotates around the axon – wrapping the axon in concentric layers of membrane = myelin sheath
More complex process for myelinated nerves, Schwann cells envelops an axon and the plasma membrane fuses to get the meson and then after fusion the plasma membrane then wraps around in concentric circles until you get a repeated layering of plasma membrane around the axon and at some point the cytoplasm can effectively be removed and then you basically just have rewearing layers of the plasma membrane wrapped around the axon
Nodes of Ranvier
Each Swann cell covers only part of an axon
Each axon in the PNS is not wrapped around by one Schwann cell we actually have many different Schwann cells that are wrapped around a particular part of the axon
Gaps where axons are not myelinated: Nodes of Ranvier
Important in signal conduction along axon
Myelin provides insulation to ensure that signals move fast along the axon and nodes of ranvier are important in conveying the signal as this is where you find the ion channels
Also found in CNS with gaps in oligodendrocyte myelination
The resting membrane potential
Having an RMP means that they can propagate APs
An electrical potential exists across the plasma membrane of all cells. The fluid inside the cell has an excess of negative charges and the fluid outside the cell an excess of positive charges.
Non-myelinated nerves are slower to conduct an action potential
They have ion channels all the way along whereas in myelinated fibres they just have ion channels in the nodes so are much quicker
Action potential of myelinated nerves quickly jumps between nodes of Ranvier
Myelination speeds up conduction velocity!
Multiple sclerosis
Autoimmune nervous system disease where immune system attacks the myelin of the CNS.
Slows down or blocks messages between the brain and the body….Causes:
Visual disturbances
Muscle weakness
Trouble with coordination and balance, numbness, prickling (“pins and needles“)
Thinking and memory problems
The cause is unknown. There is no cure for MS.
Loss of myelination in various areas of the brain and the spinal cord which is therefore responsible for the large amount of disease features
Guillain-Barre syndrome
80% of people make a full recovery
Autoimmune nervous system disease where immune system attacks the myelin of the PNS.
Loss of myelination in the PNS so get symptoms/disease features that are consistent with the loss of communication therefore tingling of hands etc
Tingling in hands and feet
Progressing weakness of limbs and respiratory muscles
Effects on autonomic nervous system lead to altered heart rate and blood pressure.
Cause unknown but usually associated with earlier infection.
Synapses
are specialised intercellular junctions which link neurons to each other and to muscles
Synaptic cleft present which is where neurotransmitters are released into so that they can be detected by ligand gated ion channels on the post synaptic cell which can continue the signal to that postsynaptic cell
Synaptic transmission at chemical synapses
Propagating axon terminates at the terminal bouton. (Axon giving the information and it terminates at a special structure called the terminal bouton)
Action potential from propagating axon elicits release of neurotransmitter from synaptic vesicles into synaptic cleft
Neurotransmitter diffuses across synaptic cleft and stimulates receptor on the postsynaptic membrane
This stimulates a response, usually an action potential, in the effector cell
Neurotransmitters include: noradrenaline, glutamate, dopamine, acetyl-choline, serotonin
neurotransmitter disorders
Neurotransmitters synthesised via biochemical pathways
Loss of enzyme GTP cyclohydrolase 1 leads to deficiency in several neurotransmitters
GTPCH deficiency Early onset (4-5 months): Intellectual disability Convulsions Irritability Hypersalivation Difficulty breathing
Treatment with neurotransmitter precursors (to regain production of the lost neurotransmitter/s)
Other deficiencies recapitulate effects
Motor neurons and NMJ
Neuromuscular junction is the synapse between motor neurons and muscle fibre
Neuromuscular junction also known as motor end plate
Specialisations from other synapses
One motor neuron can divide into many branches each ending in a neuromuscular junction - one neuron may innervate thousands of muscle fibres
NMJ
Neuromuscular junction is the synapse between motor neurons and muscle fibre
Neuromuscular junction also known as motor end plate
Motor neurons
Motor unit: Motor neuron and connected skeletal muscle fibers
Lots fibres = power
Fewer fibres = endurance ( activate different sets of motor units at different times to allow for the whole muscle to be partially contracted at different times)
Motor neurons branching to innervate a number of muscle fibres
Motor unit
Motor unit: Motor neuron and connected skeletal muscle fibers
Neuromuscular junction motor end plate process
ACh released from synaptic vesicles
Binds to nicotinic ion channels that cause membrane depolarisation
Secondary synaptic cleft causd by folding
NMJ occupies a recess on the muscle surface - sole plate
Secondary synaptic cleft allows us to have lots and lots of receptors/ion channels for the neurotransmitter so this means that there are lots of different ion channels so the membrane can be depolarised very quickly
Muscle fibre action potential
ACh released in response to AP in the motor neuron
Binds to nicotinic receptors, allowing depolarisation of sarcolemma
Action potential along sarcolemma
Into the T tubule
Calcium is released by the sarcoplasmic reticulum and it initiates muscle contraction
Myasthenia gravis
Autoimmune disease – body produces antibodies to nicotinic receptor.
Lost the ability of the nicotinic receptors to respond to ACh
Binding of acetylcholine is therefore blocked and muscle activation is inhibited.
Most commonly affected muscles: eyes, face, those associated with swallowing.
All of these are dependent on skeletal muscle fibres
Acetylcholinesterase inhibitors alleviate symptoms
This enzyme taks back up ACh out of the synaptic cleft
Immune suppressors can also help
Injecting Botox to eliminate skin wrinkles
Botulinum toxin A regulates ACh release from nerve terminals and thus selectively inhibits the underlying muscles ability to contract.
Causes chronic contraction of certain skeletal muscle fibres in the face to be inhibited
Existing lines and furrows are thus smoothed.
If too much is injected patient can end up with droopy eyelid muscles for weeks.
